Tianjin Key Laboratory of Molecular Drug Research, Tianjin International Joint Academy of Biomedicine, Tianjin, China.
Drug Safety Evaluation Center, Tianjin International Joint Academy of Biomedicine, Tianjin, China.
J Cell Mol Med. 2019 Feb;23(2):750-760. doi: 10.1111/jcmm.13897. Epub 2018 Nov 24.
In this study, we investigated the therapeutic potential of lentinan in mouse models of inflammatory bowel disease (IBD) and colitis-associated cancer (CAC). Lentinan decreased the disease activity index and macroscopic and microscopic colon tissue damage in dextran sulphate sodium (DSS)-induced or TNBS-induced models of colitis. High-dose lentinan was more effective than salicylazosulfapyridine in the mouse models of colitis. Lentinan decreased the number of tumours, inflammatory cell infiltration, atypical hyperplasia and nuclear atypia in azoxymethane/DSS-induced CAC model. It also decreased the expression of pro-inflammatory cytokines, such as IL-13 and CD30L, in IBD and CAC model mice possibly by inhibiting Toll-like receptor 4 (TLR4)/NF-κB signalling and the expression of colon cancer markers, such as carcinoembryonic antigen, cytokeratin 8, CK18 and p53, in CAC model mice. In addition, lentinan restored the intestinal bacterial microbiotal community structure in IBD model mice. Thus, it shows therapeutic potential in IBD and CAC model mice possibly by inhibiting TLR4/NF-κB signalling-mediated inflammatory responses and disruption of the intestinal microbiotal structure.
在这项研究中，我们研究了香菇多糖在炎症性肠病（IBD）和结肠炎相关癌症（CAC）小鼠模型中的治疗潜力。香菇多糖可降低葡聚糖硫酸钠（DSS）诱导或三硝基苯磺酸（TNBS）诱导的结肠炎模型中的疾病活动指数和结肠组织的宏观和微观损伤。高剂量香菇多糖在结肠炎小鼠模型中的疗效优于柳氮磺胺吡啶。香菇多糖可减少氧化偶氮甲烷/ DSS 诱导的 CAC 模型中的肿瘤数量、炎症细胞浸润、非典型增生和核异型性。它还可能通过抑制 Toll 样受体 4（TLR4）/ NF-κB 信号通路和降低 CAC 模型小鼠中结肠癌标志物（如癌胚抗原、细胞角蛋白 8、CK18 和 p53）的表达，降低 IBD 和 CAC 模型小鼠中促炎细胞因子（如 IL-13 和 CD30L）的表达。此外，香菇多糖可恢复 IBD 模型小鼠的肠道细菌微生物群落结构。因此，它可能通过抑制 TLR4/NF-κB 信号通路介导的炎症反应和破坏肠道微生物群落结构，显示出在 IBD 和 CAC 模型小鼠中的治疗潜力。
